A View from David Ewing Duncan
Can Our Genes Save Us from Our Environment?
In Science, two NIH directors declare that the time has come for a fusion of environmental science and genetics.
Why do some people end up with cancer, heart disease, or autism while others living under the same conditions don’t?
Answering this is likely to consume the life sciences for most of this century as scientists tease out the intricacies of how environmental factors turn on and off genes. (See “Why Cancer Strike Some.”) For instance, why is it that some people can be exposed to high levels of toxic chemicals, such as mercury, and remain healthy, while others suffer brain damage? More important, is there a single gene or multiple genes that protect some people from exposure to mercury? And if so, can this protector gene be used to develop methods for defending everyone against environmental scourges?
Two titans of life sciences at the National Institutes of Health (NIH) have decided that it’s time we find out. In a Science article titled “Environmental Biology and Human Disease,” Francis Collins and David Schwartz say that they believe the time has come to link two disciplines–environmental science and genetics–that have for too long operated as if they aren’t related. Collins is director of the National Human Genome Research Institute (NHGRI), and Schwartz is director of the National Institute for Environmental Health Sciences (NIEHS). The two write,
Until recently … the disciplines of environmental sciences and genetics have proceeded independently; investigators in the former discipline have focused primarily on adverse conditions and diseases that are etiologically driven by environmental factors (such as benzene-induced leukemia), and those in the latter field have been finding genetic factors for highly heritable conditions (such as cystic fibrosis). Progress is now being made in identifying common genetic variations that contribute to complex diseases such as age-related macular degeneration, type 2 diabetes, and prostate cancer. However, the best opportunity to reduce risk in genetically susceptible people for the foreseeable future will not be to re-engineer their genes, but to modify their environment.
(“Modify their environment” is a curious way to put this; I’ll get back to that in a moment.)
Collins and Schwartz call for a massive effort to record data about how, exactly, environmental factors impact genes and physiology. Part of this idea has already been launched with the Genes, Environment, and Health Initiative, which has a $40 million annual budget. “The near-term goal of the program is to develop new noninvasive tools and biomarkers for assessing individual exposures to environmental stressors that interact with genetic variation to result in human disease,” write Collins and Schwartz. They suggest that biosensors be deployed to monitor individuals’ exposure to everything from pesticides to cholesterol-rich foods. “However,” they write, “to fully appreciate the predictive importance of these measures of exposure, this technology needs to be deployed in large-scale case-control and population-based genetic studies of health and disease.”
The NIH loves big science projects, and this might be one of the biggest in history–and one of the most complex. It’s a natural outgrowth of efforts such as the Human Genome Project on the genetics side and, on the environmental side, the National Children’s Study, which, among other things, has been testing the impact of pollutants on kids.
This proposed fusion comes as global warming threatens to alter our environment and as human-produced chemicals are accumulating in the environment and in us. Last year, I was tested for 320 of these chemicals–everything from DDT to plasticizers–for an article in National Geographic, and I discovered that I have detectable levels of 165 of the chemicals. An obvious question is, what does this mean for me? Do I have genes that protect me from my rather high levels of bromide flame retardants, or are these chemicals that act as thyroid hormone disruptors slowly wreaking havoc on my physiology?
The two directors’ choice of words in this regard is interesting: they say that “the best opportunity to reduce risk in genetically susceptible people for the foreseeable future will not be to re-engineer their genes, but to modify their environment.” Modifying our environment is why you and I have these chemicals on board in the first place–and why diseases caused by junk food and other “modifiers” are raging.
We can only hope that the huge effort Collins and Schwartz are contemplating will shock us into realizing the real damage being done by such modifications to our bodies, cells, and DNA.
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